The White Army-Burns

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BURNS

Dr.Kishan Rao
• A burn is a type of injury to skin, or other tissues,
caused by heat, cold, electricity, chemicals, friction, or
radiation.
• Among women in some areas, risk is related to use of
open cooking fires or unsafe cook stoves.
• Among men, risk is related to the work environments.
Alcoholism and smoking are other risk factors.
Burns
can also occur as a result of self-harm or violence
between people.
Dupuytren’s Classification-
• First degree- Erythema then desquamation of superficial layer
of epidermis
• Second degree- Blister formation
• Third degree- Destruction of epidermis
• Fourth degree- Destruction of whole thickness of skin
• Fifth degree- Destruction of muscles
• Sixth degree- Destruction of bone, nerve trunks etc.
TYPES OF BURNS
• Thermal injury
-scald –spillage of hot liquid
-Flame burns
-Flash burns (natural gases, alcohol, combustible liquids)
-contact burns (hot meals/objects/materials)
• Electrical injury
• Chemical injury-acid/alkali
• Cold injury-frost bite
• Ionising radiation
• Sun burns
First-degree burns
• injuries confined to the epidermis.
• painful and erythematous and blanch to the touch with an
intact epidermal barrier.
• Examples include sunburn or a minor scald from a kitchen
accident. These burns do not result in scarring, and treatment
is aimed at comfort with the use of topical soothing salves
and oral nonsteroidal anti-inflammatory agents
Second-degree burns
• two types: superficial and deep.
• erythematous and painful, blanch to touch, and often blister.
• Examples include scald injuries from overheated bathtub water and flash
flame burns. These wounds spontaneously re-epithelialize from retained
epidermal structures in the rete ridges, hair follicles, and sweat glands in 1
to 2 weeks. After healing, these burns may have some slight skin
discoloration in the long term.
• Deep dermal burns into the reticular dermis appear more pale and
mottled, do not blanch to touch, but remain painful to pinprick. These
burns heal in 2 to 5 weeks by re-epithelialization from hair follicles and
sweat gland keratinocytes, often with severe scarring as a result of the
loss of dermis.
Third-degree burns
• full thickness through the epidermis and dermis and are
characterized by a hard, leathery eschar that is painless and
black,
white, or cherry red. No epidermal or dermal appendages
remain; thus, these wounds must heal by re-epithelialization
from the wound edges.
• Deep dermal and full thickness burns require excision with skin
grafting from the patient to heal the wounds in a timely
fashion

Fourth-degree burns
• involve other organs beneath the skin, such as muscle, bone,
and brain.
PATHOPHYSIOLOGY OF BURN INJURY

Local Changes
thermal injury causes coagulative necrosis of the epidermis
and underlying tissues; the depth of injury depends on the
temperature to which the skin is exposed, the specific heat of
the causative agent, and the duration of exposure.
• The area of cutaneous or superficial injury has been divided into three
zones: zone of coagulation, zone of stasis, and zone of hyperemia.
• The necrotic area of burn where cells have been disrupted is termed
the zone of coagulation. This tissue is irreversibly damaged at the time
of injury.
• The area immediately surrounding the necrotic zone has a moderate degree
of insult with decreased tissue perfusion. This is termed the zone of stasis
and, depending on the wound environment, can either survive or go on to
coagulative necrosis.
• The zone of stasis is associated with vascular damage and vessel leakage.
Thromboxane A2, a potent vasoconstrictor, is present in high
concentrations in burn wounds, and local application of inhibitors
improves blood flow and decreases the zone of stasis. Antioxidants,
bradykinin antagonists, and sub atmospheric wound pressures also
improve blood flow and affect the depth of injury.
• The last area is the zone of hyperemia, which is characterized by vasodilation from
inflammation surrounding the burn wound. This region contains the clearly viable tissue
from which the healing process begins and is generally not at risk for further necrosis.
Burn Depth
Accurate depth determination is critical to wound healing as wounds
that will heal with local treatment are treated differently from those
requiring operative intervention. Examination of the entire wound by
the physicians ultimately responsible for their managementthen is
the “gold standard” used to guide further treatment decisions. New
technologies, such as the multi sensor laser Doppler flowmeter, hold
promise for quantitative determination of burn depth.
Burn Size
• Determination of burn size estimates the extent of injury. Burn size is
generally assessed by the “rule of nines” .
• In adults, each upper extremity and the head and neck are 9% of the
total body surface area (TBSA), the lower extremities and the
anterior and posterior trunk are 18% each, and the perineum and
genitalia are assumed to be 1% of the TBSA.
• Another method of estimating smaller burns is to equate the area of
the open hand (including the palm and the extended fingers) of the
patient to be approximately 1% TBSA and then to transpose that
measurement visually onto the wound for a determination of its size.
This method is crucial in evaluating burns of mixed distribution.
• Children have a relatively larger portion of the body surface area
in the head and neck, which is compensated for by a relatively
smaller surface area in the lower extremities. Infants have 21%
of the TBSA in the head and neck and 13% in each leg, which
incrementally approaches the adult proportions with increasing
age. The Berkow formula is used to accurately determine burn
size in children
Systemic Changes
Severe burns covering more than 20% TBSA in adults and 40% TBSA in pediatric patients
are typically followed by a period of stress, inflammation, and hypermetabolism,
characterized by a hyperdynamic circulatory response with increased body temperature,
glycolysis, proteolysis, lipolysis, and futile substrate cycling. These responses are present in
all trauma, surgical, and critically ill patients, but the severity, length, and magnitude are
unique for burn patients
Hypermetabolic Response to Burn Injury
Marked and sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine
secretion are thought to initiate the cascade of events leading to the acute hypermetabolic
response with its ensuing catabolic state.
Once these cascades are initiated, their mediators and byproducts appear to stimulate the
persistent and increased metabolic rate associated with altered glucose metabolism
seen after severe burn injury.
The postburn metabolic phenomena occur in a timely manner, suggesting two
distinct patterns of metabolic regulation after injury.
• The first phase occurs within the first 48 hours of injury and has classically been
called
the ebb phase, characterized by decreases in cardiac output, oxygen consumption, and
metabolic rate as well as impaired glucose tolerance associated with its hyperglycemic
state.
• These metabolic variables gradually increase within the first 5 days after injury to a
plateau phase (called the flow phase), characteristically associated with hyperdynamic
circulation and the hypermetabolic state
Inflammation and Edema
Significant burns are associated with massive release of
inflammatory mediators, both in the wound and in other tissues.
These mediators produce vasoconstriction and vasodilation,
increased capillary permeability, and edema locally and in distant
organs.
Effects on Cardiovascular System
Microvascular changes induce cardiopulmonary alterations
characterized by loss of plasma volume, increased peripheral
vascular resistance, and subsequent decreased cardiac output
immediately after injury.
Effects on the Renal System
• Diminished blood volume and cardiac output result in
decreased renal blood flow and glomerular filtration rate.
• Other stress induced hormones and mediators, such as angiotensin,
aldosterone, and vasopressin, further reduce renal blood flow
immediately after the injury. These effects result in oliguria, which,
if left untreated, will cause acute tubular necrosis and renal failure.
Effects on the Gastrointestinal System
The gastrointestinal response to burn is highlighted by mucosal
atrophy, changes in digestive absorption, and increased intestinal
permeability. Atrophy of the small bowel mucosa occurs within 12
hours of injury in proportion to the burn size and is related to
increased epithelial cell death by apoptosis.
Effects on the Immune System
• Burns cause a global depression in immune function, which is shown
by prolonged allograft skin survival on burn wounds. Burned patients
are then at great risk for a number of infectious complications,
including bacterial wound infection, pneumonia, and fungal and viral
infections.
• These susceptibilities and conditions are based on depressed cellular
function in all parts of the immune system, including activation and
activity of neutrophils, macrophages, T lymphocytes, and B
lymphocytes. With burns of more than 20% TBSA, impairment of
these immune functions is proportional to burn size.
Which of the following statements regarding respiratory
problems in burns are true?
A. Burn injury to this function may be lethal.
B. Injury can be due to inhalation of hot or poisonous gases.
C.Burn injury is more common in the supraglottic than in the
lower airway.
D.Haemoglobin combines with carbon monoxide less easily
than with oxygen.
E. Hydrogen cyanide interferes with mitochondrial
respiration.
Ans:A, B, E
Burns can damage the airway and lungs with life-threatening
consequences. This can occur when the face or neck are burned, when
the fire causing the burn is in an enclosed space, or when hot gases or
poisonous vapours are inhaled.
Burn injury is more common in the lower airway than in the
supraglottic airway.
Carbon monoxide has an affinity 240 times greater than oxygen for
combining with haemoglobin and thus blocks the transport of oxygen.
Blood gas measurement can be done to confirm the diagnosis. A
concentration of carbon monoxide above 10 per cent is dangerous; 60
per cent is likely to be lethal.
Hydrogen cyanide is a metabolic toxin produced in house fires, which
interferes with mitochondrial respiration.
Which of the following statements regarding smoke inhalation
are true?
A.Inhaled smoke particles can cause a chemical alveolitis and
subsequent increased gaseous exchange.
B.Inhaled smoke particles may be suspected with a specific situation in
an enclosed space.
C. Early elective intubation is contraindicated.
D. Symptoms can take 24 h or up to 5 days to develop.
E.The result of carbon monoxide poisoning is a metabolic alkalosis best
treated by low inspired oxygen.
Ans: B, D
Inhaled smoke particles can cause a chemical irritation or alveolitis. This results
in interference with gaseous exchange.
Early elective intubation is important and is definitely not contraindicated.
Symptoms may not be immediately evident and can take up to 5 days to
develop.
Carbon monoxide poisoning causes a metabolic acidosis and is treated by
inhalation of pure oxygen
IMMEDIATE CARE OF THE BURN PATIENT
The principles of pre-hospital care are:
•Stop the burning proces .
•Check for other injuries. A standard ABC (airway, breathing, circulation) check followed by a
rapid secondary survey will ensure that no other significant injuries are missed.
•Cool the burn wound. This provides analgesia and slows the delayed microvascular damage that
can occur after a burn injury. Cooling should occur for a minimum of 10 minutes and is effective
up to 1 hour after the burn injury. It is a particularly important first aid step in partial-thickness
burns, especially scalds. In temperate climates, cooling should be at about 15°C, and hypothermia
must be avoided.
•Give oxygen. Anyone involved in a fire in an enclosed space should receive oxygen, especially
if there is an altered consciousness level.
•Elevate. Sitting a patient up with a burned airway may prove life-saving in the event of a delay
in transfer to hospital care. Elevation of burned limbs will reduce swelling and discomfort.
Hospital care
• A, Airway control
• B, Breathing and ventilation
• C, Circulation
• D, Disability – neurological status
• E, Exposure with environmental control
• F, Fluid resuscitation.

Major determinants of the outcome of a burn


■ Percentage surface area involved
■ Depth of burns
■ Presence of an inhalational injury
Airway
The burned airway creates problems for the patient by swelling and, if not
managed proactively, can completely occlude the upper airway. The
treatment is to secure the airway with an endotracheal tube until the swelling
has subsided, which is usually after about 48 hours. The symptoms of
laryngeal oedema, such as change in voice, stridor, anxiety and respiratory
difficulty, are very late symptoms. Intubation at this point is often difficult or
impossible owing to swelling, so acute cricothyroidotomy equipment
must be at hand when intubating patients with a delayed diagnosis of airway
burn. Because of this, early intubation of suspected airway burn is the
treatment of choice in such patients.
Initial management of the burned airway
■ Early elective intubation is safest
■ Delay can make intubation very difficult because of swelling
■Be ready to perform an emergency cricothyroidotomy, if intubation
is delayed
Breathing
Time is also a factor; anyone trapped in a fire for more than a couple of minutes
must be observed for signs of smoke inhalation. Other signs that raise suspicion
are the presence of soot in the nose and the oropharynx and a chest radiograph
showing patchy consolidation. The clinical features are a progressive increase in
respiratory effort and rate, rising pulse, anxiety and confusion and decreasing
oxygen saturation. These symptoms may not be apparent immediately and can
take 24 hours to 5 days to develop. Treatment starts as soon as this injury is
suspected and the airway is secure. Physiotherapy, nebulizers and warm
humidified oxygen are all useful. The patient’s progress should be monitored
using respiratory rate, together with blood gas measurements. If the situation
deteriorates, continuous or intermittent positive pressure may be used with a
mask or T-piece. In the severest cases, intubation and management in an intensive
care unit will be needed.
Metabolic poisoning
Any history of a fire within an enclosed space and any history of altered
consciousness are important clues to metabolic poisoning. Blood gases must be
measured immediately if poisoning is a possibility. Carboxyhaemoglobin levels
raised above 10 percent must be treated with high inspired oxygen for 24 hours
to speed its displacement from haemoglobin. Metabolic acidosis is a feature of
this and other forms of poisoning. Once again, the key to diagnosing these
injuries is suspicion from the history. Blood gas measurement will confirm the
diagnosis. The treatment is oxygen.
FLUID RESUSCITATION
The principle of fluid resuscitation is that the intravascular volume must be
maintained following a burn in order to provide sufficient circulation to perfuse
not only the essential visceral organs such as the brain, kidneys and gut, but also
the peripheral tissues, especially the damaged skin . Intravenous resuscitation is
appropriate for any child with a burn greater than 10 per cent TBSA, 15 per cent
TBSA for adults. If oral resuscitation is to be commenced, it is important that the
water given is not salt free. It is rarely possible to undergo significant diuresis in
the first 24 hours in view of the stress hormones that are present.
Hyponatraemia and water intoxication can be fatal. The resuscitation volume is
relatively constant in proportion to the area of the body burned and, therefore,
there are formulae that calculate the approximate volume of fluid needed for
the resuscitation of a patient of a given body weight with a given percentage of
the body burned. These regimens follow the fluid loss, which is at its maximum
in the first 8 hours and slows, such that, by 24–36 hours, the patient can be
maintained on his or her normal daily requirements
There are three types of fluid used. The most common is Ringer’s
lactate or Hartmann’s solution; some centres use human albumin
solution or fresh-frozen plasma, and some centres use hypertonic
saline. Perhaps the simplest and most widely used formula is the
Parkland formula. This calculates the fluid to be replaced in the
first 24 hours by the fol owing formula: total percentage body
surface area × weight (kg) × 4 = volume (mL). Half this volume
is given in the first 8 hours and the second half is given in the
subsequent 16 hours.
Crystalloid resuscitation
Ringer’s lactate is the most commonly used crystalloid. Crystalloids are said to
be as effective as colloids for maintaining intravascular volume. They are also
significantly less expensive. Another reason for the use of crystalloids is that
even large protein molecules leak out of capillaries following burn injury;
however, non-burnt capillaries continue to sieve proteins virtually normally. In
children, maintenance fluid must also be given. This is normally dextrose–
saline given as follows:
• 100 mL/kg for 24 hours for the first 10 kg;
• 50 mL/kg for the next 10 kg;
• 20 mL/kg for 24 hours for each kilogram over 20 kg body weight.
Hypertonic saline
effective in treating burns shock for many years. It produces hyperosmolarity
and hypernatraemia. This reduces the shift of intracellular water to the
extracellular space. Advantages include less tissue oedema and a resultant
decrease in escharotomies and intubations
Colloid resuscitation
Plasma proteins are responsible for the inward oncotic pressure that
counteracts the outward capillary hydrostatic pressure. Without proteins,
plasma volumes would not be maintained as there would be oedema. Proteins
should be given after the first 12 hours of burn because, before this time, the
massive fluid shifts cause proteins to leak out of the cells. The most common
colloid-based formula is the Muir and Barclay formula:
• 0.5 × percentage body surface area burnt × weight = one portion;
• periods of 4/4/4, 6/6 and 12 hours, respectively;
• one portion to be given in each period.
Monitoring of resuscitation
The key to monitoring of resuscitation is urine output. Urine output should be
between 0.5 and 1.0 mL/kg body weight per hour. If the urine output is below
this, the infusion rate should be increased by 50 per cent. If the urine output is
inadequate and the patient is showing signs of hypoperfusion (restlessness
with tachycardia, cool peripheries and a high haematocrit), then a bolus of
10 mL/kg body weight should be given. It is important that
patients are not overresuscitated, and urine output in excess of 2 mL/kg body
weight per hour should signal a decrease in the rate of infusion. Other
measures of tissue perfusion such as acid–base balance are appropriate in
larger, more complex burns, and a haematocrit measurement is a useful tool
in confirming suspected under- or overhydration. Those with cardiac
dysfunction, acute or chronic, may well need more exact measurement of
filling pressure, preferably by transoesophageal ultrasound or with the more
invasive central line
TREATING THE BURN WOUND
Escharotomy
Circumferential full-thickness burns to the limbs require emergency surgery .
One should remember that an escharotomy can cause a large amount of blood
loss; therefore, adequate blood should be available for transfusion if required.
.
Full-thickness burns and obvious deep dermal
wounds
ADDITIONAL ASPECTS OF TREATING THE BURNED PATIENT
Analgesia
Small burns, especially superficial burns, respond well to simple oral analgesia,
paracetamol and non-steroidal anti-inflammatory drugs. Topical cooling is
especially soothing. Large burns require intravenous opiates. Intramuscular
injections should not be given in acute burns over 10 per cent of TBSA, as
absorption is unpredictable and dangerous.
In patients with large burns, continuous analgesia is required, beginning with
infusions and continuing with oral tablets, such as slow-release morphine.
Powerful, short-acting analgesia should be administered before dressing
changes. Administration may require an anaesthetist, as in the case of general
anaesthesia or midazolam and ketamine, or less intensive supervision, as in the
case of morphine and nitrous oxide.
Energy balance and nutrition
One of the most important aspects in treating burns patients is nutrition. Any
adult with a burn greater than 15 per cent (10 per cent in children) of TBSA
has an increased nutritional requirement. All patients with burns of 20 per cent
of TBSA or greater should receive a nasogastric tube. (Feeding should start
within 6 hours of the injury to reduce gut mucosal damage.) A number of
different formulae are available to calculate the energy requirements of
patients
Nutrition in burns patients
■ Burns patients need extra feeding
■A nasogastric tube should be used in all patients with burns over 15 per cent
of TBSA
■ Removing the burn and achieving healing stops the catabolic drive
Monitoring and control of infection
Nursing care

Physiotherapy
All burns cause swelling,especially burns to the hands. Elevation, splintage and
exercise reduce swelling and improve the final outcome. The physiotherapy
needs to be started on day 1, so that the message can be reinforced on a daily
basis.

Psychological
A major burn is an overwhelming event, outside the normal experience, which
overwhelms the patient’s coping ability, suspends the patient’s sense of safety
and causes post-traumatic reactions. These are normal and usually self-limiting,
receding as the patient heals. The features of this intensity of experience are of
intrusive reactions, arousal reactions and avoidance reactions.
SURGERY FOR THE ACUTE BURN WOUND
• Any deep partial-thickness and full-thickness burns, except
those that are less than about 4 cm2, need surgery.
• Any burn of indeterminate depth should be reassessed after
48 hours. This is because burns that initially appear superficial
may well deepen over that time. Delayed microvascular injury
is
especially common in scalds. The essence of burns surgery
is control.
• In deep dermal burns, the top layer of dead dermis is shaved
off until punctate bleeding is observed and the dermis can be
seen to be free of any small thrombosed vessels .
MINOR BURNS/OUTPATIENT BURNS
Local burn wound care
Blisters
Whether to remove blisters or leave them intact has been the
subject of much debate. Proponents of blister removal quote
laboratory studies which show that blister fluid depresses
immune function, slowing down chemotaxis and intracellular
killing and also acting as a medium for bacterial growth.
Conversely, other authors advocate leaving blisters intact as they
form a sterile stratum spongiosum. Leaving a ruptured blister is
not advised. Initial cleaning of the burn wound Washing the burn
wound with chlorhexidine solution is ideal for this purpose.
Dressing the minor burn wound
The aims of dressing are to decrease wound pain and to protect and isolate the burn wound. The small superficial
burn
requires Vaseline gauze or another non-adherent dressing, such as Mepitel, as the first layer. Following this, gauze or
Kerlix® is wrapped around with sufficient tightness to keep the dressing intact, but not to impede the circulation. This
is further wrapped with bandage. It is important to realise that bulkiness of dressings in the minor burn wound
depends upon the amount of wound discharge. A special case is burns of the hands where dressings should be
minimised
• decrease
so as notpain
to impede
associated
mobilisation
with dressings;
and physiotherapy. Synthetic burn wound dressings are popular as they:
• improve healing times;
• decrease outpatient appointments;
• lower overall costs. Biobrane is a
bilaminar
with porcine collagendressing
and anmade
outerup of an
layer inner
of rubberised silicone impervious to gases, but not to fluids and bacteria.
Wounds tolayer of knitted
be dressed nylon
with threads
Biobrane coated
should be carefully selected. Burn wounds should be fresh (less than 24 hours),
sensate, show capillary blanching and refill. Biobrane® should be applied to the wound after removal of all blisters. It
should be checked at 48 hours for adherence and any signs of infection. It should be removed if any sign of infection is
found. Duoderm or hydrocolloid dressings are not bulky, help in healing and can be kept in place for 48–72 hours.
They provide a moist environment, which helps in re-epithelialisation of the burn wound.
Healing of burn wounds
Burns that are being managed conservatively should be healed within 3 weeks. If there are no signs of
re- epithelialisation in this time, the wound requires debridement and grafting.
Infection
Infection in the minor burn should be tackled very aggressively as it is known to
convert a superficial burn to a partial-thickness burn and a partial- to a deep partial-
thickness burn, respectively. It should be managed using a combination of topical and
systemic agents. Debridement and skin grafting should also be considered.
Itching
Most burn patients have itchy wounds. Histamine and various endopeptides are said to
be the causative factors of itching. Antihistamines, analgesics, moisturising creams,
aloe vera and antibiotics have all been tried with varying degrees of success.
Traumatic blisters
The healed burn wound is prone to getting traumatic blisters because the new
epithelium is very fragile. Non-adherent dressings usually suffice; regular
moisturisation is also useful in this condition.
NON-THERMAL BURN INJURY
Electrical injuries
Electrical injuries are usually divided into low- and high-voltage
injuries, the threshold being 1000 V
Low-tension injuries
• Low-tension or domestic appliance injuries do not have enough
energy to cause destruction to significant amounts of subcutaneous
tissues when the current passes through the body.
• The main danger with these injuries is from the alternating current
interfering with normal cardiac pacing. This can cause cardiac arrest.
The electricity itself does not usually cause significant underlying
myocardial damage, so resuscitation, if successful, should be lasting.
High-tension injuries
• High-tension electrical injuries can be caused by one of three sources
of damage: the flash, the flame and the current itself.
• When a high-tension line is earthed, enormous energy is released as
the current travels from the line to the earth. It can arc over the
patient, causing a flash burn. The extremely rapid heating of the air
causes an explosion that often propels the victim backwards. The
key
here is that the current travelled from the line to the earth directly
and not through the patient.
• The flash, however, can go on to ignite the patient’s clothes and so
cause a normal flame burn.The damage to the underlying muscles in
the affected limb can cause the rapid onset of compartment syndrome.
The release of the myoglobins will cause myoglobinuria and
subsequent renal dysfunction. Therefore, during the resuscitation of
these patients, efforts must be made to maintain a high urine output of
up to 2 mL/kg body weight per hour. Severe acidosis is common in
large electrical burns and may require boluses of bicarbonate.
• These patients are also at risk of myocardial damage as a result of
direct muscle damage rather than by interference with cardiac pacing.
This gives rise to significant electrocardiogram changes, with raised
cardiac enzymes. In the case of a severe injury through a limb, primary
amputation is sometimes the most effective management.
Chemical injuries
• There are two aspects to a chemical injury. The first is the physical
destruction of the skin and the second is any poisoning caused by
systemic absorption.
• The initial management of any chemical injury is copious
lavage with water. There are only a handful of chemicals for
which water is not helpful, for example phosphorus, which is a
component of
some military devices, and elemental sodium, which is
occasionally present in laboratory explosions. These substances
need to be physically removed with forceps.
• Alkalis are usually the more destructive and are especially dangerous if
they have come into contact with the eyes. After copious lavage, the
next step in the management of any chemical injury is to identify the
chemical and its concentration and to elucidate whether there is any
underlying threat to the patient’s life if absorbed systemically. One acid
that is a common cause of acid burns is hydrofluoric acid.
• The initial management is with calcium gluconate gel topically;
however, severe burns or burns to large areas of the hand can be
subsequently treated with Bier’s blocks containing calcium gluconate
10 per cent. If the patient has been burnt with a concentration greater
than 50 per cent, the threat of hypocalcaemia and subsequent
arrhythmias then becomes high, and this is an indication for acute early
excision.
• It is best not to split-skin graft these hydrofluoric acid wounds initially,
but to do this at a delayed stage
Ionising radiation injury
The management of localised radiation damage is usually conservative
until the true extent of the tissue injury is apparent. Should this damage
have caused an ulcer, then excision and coverage with vascularised
tissue is required. A patient who has suffered whole-body irradiation
and is suffering from acute desquamation of the skin has received a
lethal dose of radiation, which can cause a particularly slow and
unpleasant death. Non lethal radiation has a number of systemic effects
related to the gut mucosa and immune system dysfunction.
Cold injuries
• Cold injuries are principally divided into two types: acute cold injuries
from industrial accidents and frostbite.
• Exposure to liquid nitrogen and other such liquids will cause epidermal
and dermal destruction. The tissue is more resistant to cold injury than
to heat injury, and the inflammatory reaction is not as marked. The
assessment of depth of injury is more difficult.
• Frostbite injuries affect the peripheries in cold climates. The initial
treatment is with rapid rewarming in a bath at 42°C. The cold injury
produces delayed microvascular damage similar to that of cardiac
reperfusion injury. The level of damage is difficult to assess, and
surgery usually does not play a role in its management, which is
conservative, until there is absolute demarcation of the level of injury.
References
1.Bailey and love’s short practice of surgery
2.Sabiston’s textbook of surgery
3. Schwartz principles of surgery
4. Textbook of plastic surgery- grabbe and
smith

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